Attenuation of Vasospasm by Dexmedetomidine after Experimental Subarachnoidal Haemorrhage in Rabbits

Aim: Vasospasm is one of the most important factors that influence the successful treatment of ruptured intracranial aneurysm. We studied if vasospasm following subarachnoidal haemorrhage (SAH) can be alleviated by dexmedetomidine in an animal model. Materials and Methods: Experimental SAH was induced in 12 of 18 New Zealand rabbits by intracisternal injection of autologous blood. Control animals (sham SAH, n = 6) received intracisternal injection of the respective volume of physiological saline solution. Forty eight hours after the operation, rabbits in sham SAH and SAH-alone (n = 6) groups were infused intravenously with 0.9% sodium chloride for 2 h, whereas rabbits in SAH-dexmedetomidine group (n = 6) received intravenous infusion of 5 µg/kg per h dexmedetomidine for 2 h. All rabbits were sacrificed with penthotal 24 h after infusions. Basilar arteries were isolated and processed for histology. Results: The histological specimens revealed evidence of arterial narrowing and vascular wall thickening in both SAH-alone and SAH-dexmedetomidine groups. The wall thickness of basilar artery significantly increased and lumen diameter significantly reduced in SAH-alone group in comparison with basilar arteries from other groups (P < 0.05). SAH-dexmedetomidine group revealed attenuation of vasospasm formed after 72 h. Conclusions: Our study showed that vasospasm is attenuated by dexmedetomidine administered after vasospasm is formed in a rabbit model.

Attenuation of Vasospasm by Dexmedetomidine after Experimental Subarachnoidal Haemorrhage in Rabbits

Aim: Vasospasm is one of the most important factors that influence the successful treatment of ruptured intracranial aneurysm. We studied if vasospasm following subarachnoidal haemorrhage (SAH) can be alleviated by dexmedetomidine in an animal model. Materials and Methods: Experimental SAH was induced in 12 of 18 New Zealand rabbits by intracisternal injection of autologous blood. Control animals (sham SAH, n = 6) received intracisternal injection of the respective volume of physiological saline solution. Forty eight hours after the operation, rabbits in sham SAH and SAH-alone (n = 6) groups were infused intravenously with 0.9% sodium chloride for 2 h, whereas rabbits in SAH-dexmedetomidine group (n = 6) received intravenous infusion of 5 µg/kg per h dexmedetomidine for 2 h. All rabbits were sacrificed with penthotal 24 h after infusions. Basilar arteries were isolated and processed for histology. Results: The histological specimens revealed evidence of arterial narrowing and vascular wall thickening in both SAH-alone and SAH-dexmedetomidine groups. The wall thickness of basilar artery significantly increased and lumen diameter significantly reduced in SAH-alone group in comparison with basilar arteries from other groups (P < 0.05). SAH-dexmedetomidine group revealed attenuation of vasospasm formed after 72 h. Conclusions: Our study showed that vasospasm is attenuated by dexmedetomidine administered after vasospasm is formed in a rabbit model.

___

  • 1. Wilkins RH. Attempted prevention or treatment of intracranial arterial spasm: a survey. Neurosurgery 1980; 6:198-210.
  • 2. Atalay B, Bolay H, Dalkara T. Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a non invasive method to activate the trigeminovascular reflex. J Neurosurg 2002; 97: 1179-1183.
  • 3. Aydın IH, Onder A. The effect of very early cisternal irrigatio on basilar artery spasm SAH in rat model. Acta Neurochir (Wien) 1991; 113: 69-73.
  • 4. Bagirici F, Bostanci MO. Anticonvulsive effects of nimodipine on penicillin-induced epileptiform activity. Acta Neurobiol Exp (Wars) 2006; 66 (2): 123-128.
  • 5. Kemaloglu S, Ozkan U, Yilmaz F. Preventive effects of intracisternal alphatocopherol on cerebral vasospasm in experimental subarachnoid haemorrhage. Yonsei Med J 2003; 44: 955-960.
  • 6. Mayberg MR, Okada T, Bark HD. The significance of morphological changes in cerebral arteries after subarachnoid haemorrhage. J Neurosug 1990; 72: 626-633.
  • 7. Munoz-Castaneda JR, Montilla P, Padillo FJ, Bujalance I, Munoz MC, Muntane J, Tunez I . Role of serotonin in cerebral oxidative stress in rats. Acta Neurobiol Exp (Wars) 2006; 66 (1): 1-6.
  • 8. Naredi S, Lambert G, Eden E. Increased sympathetic nervous activity in patients with nontraumatic subarachnoid hemorrhage. Stroke 2000; 31: 901–906.
  • 9. Hoffman WE, Kochs E, Werner C. Dexmedetomidine improves neurologic outcome from incomplete ischemia in the rat. Anesthesiology 1991; 75: 328-332.
  • 10. Maeir C, Steinberg GK, Sun GH. Neuroprotection by the α-2 adrenoceptor agonist dexmedetomidine in a focal model of cerebral ischemia. Anesthesiology 1993; 79: 1-7.
  • 11. Kuhmonen J, Pokorny J, Miettinen R. Neuroprotective effects of of dexmedetomidine in the gerbil hippocampus following transient global ischemia. Anesthesiology 1997; 87: 371-377.
  • 12. Karlsson BR, Löberg EM, Steen PA. Dexmedetomidine, a potent α2-agonist, does not affect neuronal damage following severe forebrain ischemia in the rat. Eur J Anesthesiol 1995; 12:281- 285.
  • 13. Bunc G, Kovacic S, Strnad S. Attenuation of cerebral vasospasm in rabbits using clonidine hydrochloride, a central adrenergic agonist. Autonomic Neuroscience: Basic and Clinical 2003; 105: 71–76.
  • 14. Matsumoto M, Zornow MH, Rabin BC, Maze M. The α–adrenergic agonist, dexmedetomidine, selectively attenuates is- 2 chemia-induced increases in striatal norepinephrine concentrations. Brain Res 1993; 627: 325–329.
  • 15. Peerless SJ, Yasargil MG. Adrenergic innervation of the cerebral blood vessels in the rabbit. J Neurosurg 1971; 35: 148–154.
  • 16. Solomon RA, Antunes JL, Chen RYZ. Decrease in cerebral blood flow in rats after experimental subarachnoid heamorrhage: A new model. Stoke 1985;16: 58-64.
  • 17. Jolkkonen J, Puurunen K, Koistinaho J, Kauppinen R, Haapalinna A, Nieminen L, Sivenius J. Neuroprotection by the α2- adrenoceptor agonist, dexmedetomidine, in rat focal cerebral ischemia. Eur J Pharm 1999; 372: 31-36.
  • 18. Lobato RD, Marin J, Salaices M. Cerebrovascular reactivity to noradrenaline and serotonin following experimental subarachnoid hemorrhage. J Neurosurg 1980; 53: 480–485.
  • 19. Minegishi A, Ishizaki T, Yoshida Y. Plasma monoaminergic metabolites and catecholamines in subarachnoid hemorrhage: Clinical implications. Arch Neurol 1987; 44: 423-428.
  • 20. Hamann G, Haass A, Schimrigk K. Beta-blockade in acute aeurysmal subarachnoid hemorrhage. Acta Neurochir 1993; 121: 119-122.
  • 21. Bunc G, Kovacic S, Strnad S. Sympathetic nervous system exclusion following experimental subarachnoid haemorrhage prevents vasospasm in rabbits. Wien Klin Wochenschchr 2000; 112: 533-539.
  • 22. Lambert G, Naredi S, Edin E. Sympathetic nervous activation following subarachnoid hemorrhage: Influence of intravenous clonidine Acta Anaesthesiol Scand 2002; 46: 160-165.
  • 23. Tsukahara T, Taniguchi T, Usui H. Sympathetic denervation and alpha adrenoceptors in dog cerebral arteries. Naunyn Schmiedebergs Arch Pharmacol 1986; 334: 436–443.
  • 24. Iida H, Iida M, Ohata H, Nagase K, Dosi H. Hypothermia Attenuates the Vasodilator Effects of Dexmedetomidine on Pial Vessels in Rabbits In Vivo. Anesth Analg 2004; 98: 477-482.
  • 25. Zornow MH, Fleischer JE, Scheller MS. Dexmedetomidine, an alpha 2-adrenergic agonist, decreases cerebral blood flow in the isoflurane-anesthetized dog. Anesth Analg 1990; 70: 624–630.
  • 26. Ohata H, Iida H, Dohi S. Intravenous dexmedetomidine inhibits cerebrovascular dilation induced by isoflurane and sevoflurane in dogs. Anesth Analg 1999; 89: 370–377.
  • 27. Prielipp RC, Wall MH, Tobin JR. Dexmedetomidine-induced sedation in volunteers decreases regional and global cerebral blood flow. Anesth Analg 2002; 95: 1052–1059.
  • 28. Bryan RM Jr, Eichler MY. Stimulation of alpha 2 adrenoceptors dilates the rat middle cerebral artery. Anesthesiology 1996; 85: 82–90.
  • 29. Cooke JP. Does ADMA cause endothelial dysfunction? Arterioscler Thromb Vasc Biol 2000; 20: 2032–2037.
  • 30. Kovacic S, Bunc G, Ravnik J. Correspondance between the time course of cerebral vasospam and the level of cerebral dopamine- α-hydroxylase in rabbits. Auton Neurosci 2006; 130: 28-31
Turkish Journal of Medical Sciences-Cover
  • ISSN: 1300-0144
  • Yayın Aralığı: Yılda 6 Sayı
  • Yayıncı: TÜBİTAK
Sayıdaki Diğer Makaleler

Is MEFVGene Arg202Gln (605 G>A) A Disease-Causing Mutation?

Ayşenur ÖZTÜRK, Birsin ÖZÇAKAR, Mesiha EKİM, Nejat AKAR

Elective Treatment of Detorsioned Sigmoid Volvulus

Mahmut BAŞOĞLU, Bülent AYDINLI, Gürkan ÖZTÜRK, M.İlhan YILDIRGAN, K.Yalçın POLAT, Durkaya ÖREN, S.Selçuk ATAMANALP, Mecit KANTARCI, Ahmet A. BALIK

Structural Changes of Placenta in Preeclamptic Patients: Light and Electron Microscopic Study

Mohamed Abdel Monem DKHIL, Reda Awadallah SALEH

Antimicrobial Susceptibility of Brucella melitensis Isolates from Blood Samples

Sedat KAYGUSUZ, Ergin AYAŞLIOĞLU, Selçuk KILIÇ, Kemalettin AYDIN, Dilek KILIÇ, Canan AĞALAR

A Rare Cause of Intestinal Obstruction: Meckel´s Diverticulitis

Oskay KAYA, Münevver MORAN, Fatih ÖZDEMİR, Süleyman ÇETİNKUNAR

Gastrointestinal Stromal Tumor with Pulmonary Metastasis

Eren ERSOY, Bülent DEMİRBAŞ, Selma GÖĞKUŞ, Raci AYDIN, Ahmet GÜRER

The Association of D-Dimer Levels with Other Prognostic Factors in Patients with Lung Cancer

Nuri KARADURMUŞ, Okan KUZHAN, Kudret EKİZ, Cantürk TAŞÇI, Ahmet ÖZET, Satılmış İNAL, Arzu BALKAN, Metin ÖZKAN, Hayati BİLGİÇ

Is MEFV Gene Arg202Gln (605 G>A) a disease-causing mutation?

Birsin ÖZÇAKAR, Mesiha EKİM, Nejat AKAR, Ayşenur ÖZTÜRK

Second-Line Drug Susceptibilities of Multidrug-Resistant Mycobacterium tuberculosis Isolates in Aegean Region - Turkey

Nuri ÖZKÜTÜK, Aydan ÖZKÜTÜK, Hörü GAZİ, Beril ÖZBAKKALOĞLU, Süheyla SÜRÜCÜOĞLU, Meral COŞKUN

Transient Fetal and Neonatal Ascites: A New Finding of Down Syndrome?

Mustafa Mansur TATLI, Semra KARA, Nurdan URAS, Alpaslan TANBUL, Melike METİN, Tuğba HALICI, Ahmet KARADAĞ